scholarly journals Increased expression of both short and long forms of prolactin receptor mRNA in hypothalamic nuclei of lactating rats

1999 ◽  
Vol 23 (1) ◽  
pp. 13-22 ◽  
Author(s):  
XJ Pi ◽  
DR Grattan
Keyword(s):  
Short Form ◽  
Post Partum ◽  
Prolactin Receptor ◽  
Brain Regions ◽  
Physiological Changes ◽  
Receptor Mrna ◽  
Reverse Transcription Pcr ◽  
Hypothalamic Nuclei ◽  
Long Form ◽  
The Brain

This study investigated expression of prolactin receptor (PRL-R) mRNA in selected hypothalamic nuclei of lactating rats (days 7-10 post partum) compared with dioestrous rats. Rat brains were frozen with liquid nitrogen and cut into coronal sections of 300 microm. From these sections, tissues were micropunched from the parietal cortex (CTX), choroid plexus (ChP), and five hypothalamic regions: supraoptic (SO), paraventricular (Pa), arcuate (Arc) and ventromedial hypothalamic (VMH) nuclei, and median eminence (ME). Expression of both short and long forms of PRL-R mRNA were evaluated by reverse transcription-PCR and Southern hybridisation. The results showed that the relative amount of short form mRNA in the ChP of lactating rats was significantly higher than in dioestrous rats. The short form of PRL-R mRNA was undetectable in the SO, Pa, VMH of dioestrous rats but was expressed at a significant level in lactating rats. Levels of long form mRNA in the ChP, SO, Pa and VMH in lactating rats were significantly increased compared with dioestrous rats. Moreover, the long form mRNA was induced in the CTX of lactating rats. In the Arc, levels of both forms of PRL-R mRNA tended to increase in lactating rats compared with dioestrous rats but changes were not statistically significant. Neither form of PRL-R mRNA was detectable in the ME in the two animal models. Increased expression of PRL-R mRNA in specific brain regions during lactation is consistent with the variety of PRL effects on the brain, and may help to explain profound physiological changes in the lactating mother.

scholarly journals Quantitation of prolactin receptor mRNA in the maternal rat brain during pregnancy and lactation

2003 ◽  
Vol 31 (1) ◽  
pp. 221-232 ◽  
Author(s):  
RA Augustine ◽  
IC Kokay ◽  
ZB Andrews ◽  
SR Ladyman ◽  
DR Grattan
Keyword(s):  
Choroid Plexus ◽  
Time Course ◽  
Short Form ◽  
Prolactin Receptor ◽  
Female Rats ◽  
Mrna Levels ◽  
Receptor Mrna ◽  
Hypothalamic Nuclei ◽  
Long Form ◽  
Pregnancy And Lactation

Prolactin receptor (PRL-R) expression in the brain is increased in lactating rats compared with non-pregnant animals. The aim of the present study was to determine the time-course of changes in PRL-R mRNA levels during pregnancy and/or lactation, and to determine relative levels of the two forms (short and/or long form) of receptor mRNA in specific brain regions. Brains were collected from female rats on dioestrus, days 7, 14 or 21 of pregnancy, day 7 of lactation or day 7 post-weaning. Frozen, coronal sections were cut (300 microm) and specific hypothalamic nuclei and the choroid plexus were microdissected using a punch technique. Total RNA was extracted and reverse transcribed, then first strand cDNA was amplified using quantitative real-time PCR. Results showed an up-regulation of long-form PRL-R mRNA in the choroid plexus by day 7 of pregnancy compared with dioestrus, which further increased on days 14 and 21 of pregnancy and day 7 of lactation, and then decreased to dioestrous levels on day 7 post-weaning. Short-form PRL-R mRNA levels increased on day 14 of pregnancy relative to dioestrus, increased further on day 7 of lactation and decreased on day 7 post-weaning. Changes in mRNA were reflected in increased levels of PRL-R immunoreactivity in the choroid plexus during pregnancy and lactation, compared with dioestrus. In the arcuate nucleus, long-form PRL-R mRNA was increased during pregnancy. In contrast to earlier work, no significant changes in short- or long-form PRL-R mRNA expression were detected in several other hypothalamic nuclei, suggesting that changes in hypothalamic mRNA levels may not be as marked as previously thought. The up-regulation of PRL-R mRNA and protein expression in the choroid plexus during pregnancy and lactation suggest a possible mechanism whereby increasing levels of peripheral prolactin during pregnancy may have access to the central nervous system. Together with expression of long-form PRL-R mRNA in specific hypothalamic nuclei, these results support a role for prolactin in regulating neuroendocrine and behavioural adaptations in the maternal brain.

Preferential expression of long form prolactin receptor mRNA in the rat brain during the oestrous cycle, pregnancy and lactation: hormones involved in its gene expression

1994 ◽  
Vol 141 (2) ◽  
pp. 325-333 ◽  
Author(s):  
T Sugiyama ◽  
H Minoura ◽  
N Kawabe ◽  
M Tanaka ◽  
K Nakashima
Keyword(s):  
Rat Brain ◽  
Short Form ◽  
Prolactin Receptor ◽  
Mrna Level ◽  
Oestrous Cycle ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
Long Form ◽  
Pregnancy And Lactation ◽  
The Brain

Abstract The mRNA species for prolactin receptor (PRL-R) isoforms, long and short form PRL-Rs, were estimated by the reverse transcription-polymerase chain reaction method in the rat brain (cerebrum) during the oestrous cycle, pregnancy and lactation. The levels of long form PRL-R mRNA increased at pro-oestrus and oestrus, at the same time as serum prolactin levels increased, whereas the mRNA level of short form PRL-R was relatively unchanged. Long form PRL-R mRNA expression was also markedly increased in the brain at mid- and late gestation, and this elevated mRNA level was maintained during the period of lactation. In contrast, basal levels of short form PRL-R mRNA were also maintained throughout these periods of gestation and lactation. Ovariectomy moderately reduced brain mRNA levels of both long and short form PRL-R from the levels of those in control dioestrous rats, and hypophysectomy further suppressed them to the lowest levels. Administration of oestradiol valerate (E2V) or 17α-hydroxyprogesterone caproate (17OHPC) to ovariectomized rats resulted in dramatic increases in long form PRL-R mRNA levels in the brain, whereas no significant increase in short form PRL-R mRNA was observed. In rats which were ovariectomized and hypophysectomized, the administration of 17OHPC, rat prolactin or rat GH partially restored the brain level of long form PRL-R mRNA but not short form PRL-R mRNA. E2V, on the other hand, had no effect on the expression of brain PRL-R mRNAs in these hypophysectomized rats, suggesting that the stimulatory effect of E2V on long form PRL-R mRNA expression in ovariectomized rats was mediated by an enhanced secretion of a pituitary hormone, prolactin. These results suggest that the expression of long form PRL-R mRNA in the rat brain is directly induced by progesterone, prolactin or GH during the oestrous cycle, pregnancy and lactation. Journal of Endocrinology (1994) 141, 325–333

Visualization of gene expression of short and long forms of prolactin receptor in rat digestive tissues

1994 ◽  
Vol 266 (5) ◽  
pp. G807-G815 ◽  
Author(s):  
A. Ouhtit ◽  
P. A. Kelly ◽  
G. Morel
Keyword(s):  
Gene Expression ◽  
Gastrointestinal Tract ◽  
Short Form ◽  
Receptor Gene ◽  
Prolactin Receptor ◽  
High Signal ◽  
Long Form ◽  
Receptor Gene Expression ◽  
Receptor Mrnas

Several effects of prolactin have been characterized in various tissues of the gastrointestinal tract. In the present study, the expression of short and long forms of prolactin receptor was explored and quantified in the digestive tract and correlated to the prolactin specific functions. Sections of all digestive tissues were analyzed by in situ hybridization, using 35S-labeled oligoprobes unique to each form of receptor. Macroautoradiogram signals were quantified and expressed in arbitrary units. In rat liver, prolactin receptor mRNAs are expressed to a much greater degree in females than in males. The short-form transcript is significantly expressed to a greater degree in liver, whereas the long form predominates in the pancreas and esophagus. In the remainder of the gastrointestinal tract, there is an equivalent distribution of short- and long-form transcripts. Relatively high signal intensities are seen in the stomach, duodenum, jejunum, ileum, and colon, whereas the rectum is essentially negative. The identification of prolactin receptor gene expression to limited regions should help establish specific functions associated with this hormone in the digestive tissues.

scholarly journals Downregulation of long-form prolactin receptor mRNA during prolactin-induced luteal regression

2000 ◽  
pp. 285-292 ◽  
Author(s):  
JM Bowen ◽  
CM Telleria ◽  
R Towns ◽  
PL Keyes
Keyword(s):  
Internal Control ◽  
Short Form ◽  
Prolactin Receptor ◽  
Chorionic Gonadotrophin ◽  
Corpora Lutea ◽  
Rt Pcr ◽  
Dominant Form ◽  
Receptor Isoforms ◽  
Long Form ◽  
Design And Methods

OBJECTIVE: Prolactin is capable of both trophic and lytic actions in rat corpora lutea. In corpora lutea responding to a trophic prolactin signal, the long form of the prolactin receptor is the dominant form and is upregulated by prolactin. We investigated whether mRNA for the short form of the prolactin receptor was dominant in corpora lutea responding to a lytic prolactin signal, and whether the relative concentrations of the mRNAs for both forms of the prolactin receptor were changed during this response. DESIGN AND METHODS: Immature rats were ovulated by injection of 5 IU equine chorionic gonadotrophin and 5 IU human chorionic gonadotrophin, and were hypophysectomized shortly after ovulation. Nine days after hypophysectomy, rats were injected with prolactin (500 microg/day) or vehicle for 24 (n=6, n=6) or 72 h (n=13, n=5). Total RNA was isolated from corpora lutea and mRNA for both types of prolactin receptor were analyzed by semiquantitative RT-PCR using the ribosomal protein S16 as the internal control. RESULTS: The intensities of the long- and short-form prolactin receptor signals were normalized to the S16 internal control and expressed as relative densitometric units. The normalized values at 24h for prolactin-treated vs vehicle-treated rats were 0.23 +/- 0.05 vs 0.49 +/- 0.15 (P>0.05) for the short form and 4.04 +/- 0.8 vs 4.23 +/- 0. 6 (P>0.05) for the long form. The values for 72 h were 0.30 +/- 0.05 vs 0.24 +/- 0.05 (P>0.05) for the short form and 2.76 +/- 0.4 vs 5. 53 +/- 0.3 (P<0.01) for the long form respectively. CONCLUSION: The long form of the prolactin receptor is the dominant form at both time-points; however, the concentration of mRNA for this receptor isoform was specifically downregulated by prolactin treatment. Our results suggest that the short form of the prolactin receptor alone is unlikely to mediate the luteolytic action of prolactin, but that luteolytic events may be influenced via a change in the ratio of the two receptor isoforms.

scholarly journals Characterization of multiple first exons in murine prolactin receptor gene and the effect of prolactin on their expression in the choroid plexus

2012 ◽  
Vol 48 (2) ◽  
pp. 169-176 ◽  
Author(s):  
Hidemi Tabata ◽  
Momoko Kobayashi ◽  
Junko H Ikeda ◽  
Nobuhiro Nakao ◽  
Toru R Saito ◽  
...  
Keyword(s):  
Gene Expression ◽  
Choroid Plexus ◽  
Transcriptional Activation ◽  
Short Form ◽  
Receptor Gene ◽  
Prolactin Receptor ◽  
Brain Regions ◽  
Expression Level ◽  
Expression Levels ◽  
A Site

Prolactin (Prl) receptor (Prlr) gene is expressed in various brain regions, with the highest level present in the choroid plexus, a site for receptor-mediated PRL transport from the blood to cerebrospinal fluid. We investigated the regulatory mechanism ofPrlrgene expression by PRL in the murine choroid plexus. We first examined the organization of the alternative first exons in murinePrlrgene. In addition to the three known first exons, mE11, mE12, and mE13, two first exons, mE14and mE15, were newly identified by cDNA cloning. Each first exon variant ofPrlrmRNA exhibited tissue-specific or generic expression. In the choroid plexus of mice, the expression levels ofmE13-,mE14-, andmE15-PrlrmRNAs were increased in the lactating mice compared with those in the diestrus mice. Furthermore, the expression level ofmE14-PrlrmRNA was decreased in the PRL-deficient (Prl−/−) mice compared with the PRL-normal (Prl+/+andPrl+/−) mice. In the ovariectomizedPrl−/−mice, the expression level ofmE14-PrlrmRNA was significantly increased by PRL administration but not by 17β-estradiol administration. The expression levels of the two last exon variants ofPrlrmRNAs, encoding the long and short cytoplasmic regions of PRLR, were also increased in the lactating mice and decreased in thePrl−/−mice. These findings suggest that PRL stimulates thePrlrgene expression through the transcriptional activation of mE14first exon, leading to increases in the long- and short-form variants ofPrlrmRNA in the murine choroid plexus.

Pup contact induces the expression of long form prolactin receptor mRNA in the brain of female rats: effects of ovariectomy and hypophysectomy on receptor gene expression

1996 ◽  
Vol 149 (2) ◽  
pp. 335-340 ◽  
Author(s):  
T Sugiyama ◽  
H Minoura ◽  
N Toyoda ◽  
K Sakaguchi ◽  
M Tanaka ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Choroid Plexus ◽  
Prolactin Receptor ◽  
Female Rats ◽  
Maternal Behaviour ◽  
Mrna Levels ◽  
Female Rat ◽  
Expression Levels ◽  
Long Form ◽  
The Brain

Abstract Prolactin receptor (PRL-R) mRNA expression levels in the female rat brain (cerebrum) during pup contact stimulation were determined by the reverse transcription-PCR method. The high expression levels of long form PRL-R mRNA found in the brain of lactating rats were markedly reduced by removal of pups, and long form PRL-R mRNA levels were recovered by resumption of pup contact. Interestingly, pup contact stimuli of nulliparous virgin rats also markedly induced long form but not short form PRL-R mRNA expression in the brain in 1·3 days, together with the expression of maternal behaviour. In ovariectomized (OVX) or hypophysectomized (HYPOX) virgin rats, or in OVX plus HYPOX virgin rats, however, brain long form PRL-R mRNA was not significantly induced by pup contact stimuli for as long as 7 days, while maternal behaviour was fully expressed in these rats after 7 days of pup contact. The in situ hybridization experiments revealed that the long form PRL-R mRNA induced in virgin rats in contact with pups or in lactating rats was localized in the epithelial cells of the choroid plexus. No significant increase in mRNA was detected in other regions of the brain, such as the hypothalamus or cortex, in these maternal female rats. These results suggest that pup contact induces the expression of long form PRL-R mRNA in the choroid plexus of the brain in the presence of female sex steroid and pituitary hormones for the rapid expression of maternal behaviour. Our studies also suggested that maternal behaviour can be expressed in OVX or HYPOX rats after exposure to pups for 7 days without any significant increase in brain PRL-R mRNA expression. Journal of Endocrinology (1996) 149, 335–340

scholarly journals Short form 1b human prolactin receptor down-regulates expression of the long form

2009 ◽  
Vol 44 (3) ◽  
pp. 187-194 ◽  
Author(s):  
Dunyong Tan ◽  
Ameae M Walker
Keyword(s):  
Fluorescent Protein ◽  
Luciferase Activity ◽  
Short Form ◽  
Prolactin Receptor ◽  
Cell Number ◽  
293 Cells ◽  
Gfp Fluorescence ◽  
Long Form ◽  
Human Prolactin ◽  
Green Fluorescent

Alternative splicing produces different human prolactin (PRL) receptors. These include a long form (LF) and two short forms (SF1a and SF1b). The SFs of the receptor can act as dominant negatives for PRL effector function through the LF. This is proposed to be due to LF–SF heterodimerization and resultant interference with LF–LF dimer signaling. We, along with others, have provided evidence for LF–SF heterodimerization of the human receptors in support of this mechanism, along with others. However, to further investigate the ways SF may influence LF function, we co-transfected human embryonic kidney 293 cells with vectors coding for tagged (green fluorescent protein (GFP) or luciferase) LF alone or plus untagged SF1b and measured LF-GFP intensity, LF-luciferase activity, and LF mRNA 48 h later. Equal amounts of SF1b cDNA decreased LF-GFP fluorescence intensity, LF-luciferase activity, and LF mRNA by 80–100%. Similar co-transfections with untagged LF had no significant effect on tagged LF expression. Use of hygromycin showed degradation of already formed protein was the same for LF-luciferase alone and LF-luciferase with SF1b. Inhibition of mRNA synthesis, on the other hand, showed that SF1b expression accelerated LF mRNA degradation two- to three-fold. SF1b also down-regulated expression of endogenous LF mRNA in T47D breast cancer cells and opposed an increase in cell number resulting from transfection with extra LF alone. These results demonstrate a previously unrecognized mechanism whereby SF1b affects the end result of signaling through the LF receptor. The effects on cell number also support the concept that the LF:SF1b ratio may be relevant to tumor growth.

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